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Mathiastheok
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I am sure most if not all of you are aware of the current research with Myostatin and when hindered (via a cellular protein docking point) the ability of muscles to grow unhindered (albiet much greater with stimulus..ie exercise).
There is another drug in development which hopes to prevent atrophy, or muscle loss. Which would be a perfect complimet to a myostatin inhibitor.
So imagine coupiling a potential myostatin inhibitor allowing your muscles to grow without the hinderance of myostatin, AND have the atrophy of muscles not work or unused slowed tremendously. A beautiful combination.
(As a note, there currently are no drugs or supliments on the market that can inhibit myostatin. Wyeth pharmacuticals is currently in stage 2 FDA trials of a myostatin inhibitor. It is a pill that disolves in the body...myostatin is a type of protein and the pill is a cellular docking point for the myostatin protein..basically it disolves in the body to "collect" the myostatin..and with less myostatin, muscles have no restrictions on growth from myostatin. Any company claiming to have a myostatin inhibitor is completley fradulent at this time)
Researchers in Purdue University's School of Medicine have discovered genetic and drug-treatment methods to arrest the type of muscle atrophy often caused by muscle disuse, as well as aging and diseases such as cancer.
The findings might eventually benefit people who have been injured or suffer from diseases that cause them to be bedridden and lose muscle mass, or sometimes limbs, due to atrophy, said Amber Pond, a research scientist in the school's Department of Basic Medical Sciences.
"We've found a chemical 'switch' in the body that allows us to turn atrophy on, and, from that, we also have learned how to turn atrophy off."
A protein called Merg1a plays a key role in allowing or blocking muscle atrophy and atrophy can be blocked by an antihistamine which targets Merg1a and also by gene therpy.
The research team found atrophy of skeletal muscle in mice could be inhibited with both gene therapy and drug treatment using astemizole (as-TEM-uh-zole), an antihistamine. This new insight has potential in many different areas of research, Pond said.
"We have discovered a direct link between atrophy and a protein in the skeletal muscle," Pond said. "This led us to develop methods that would block the protein's ability to cause atrophy. Through drug treatment, we were able to block atrophy, allowing muscle to retain 97 percent of its original fiber size in the face of atrophy."
While the drug used in the experiment isn't suitable for human use this discovery points toward a direction for drug development to prevent muscle atrophy with cancer, age, or low exercise.
A mutant form of Merg1a inserted with gene therapy prevented muscle atrophy in low exercise mice.
This method allowed the scientists to demonstrate the effects of skeletal muscle atrophy and investigate reasons for the link with the Merg1a protein. The Merg1a protein is a channel that normally passes a small electrical current across the cell.
The researchers implanted a gene into the skeletal muscle that resulted in a mutant form of this protein that combines with the normal protein and stops the current. The researchers found that the mutant protein would inhibit atrophy in mice whose ability to use their back legs was limited.
Because gene therapy is not yet a practical treatment option in humans, the researchers decided to go a step further and stop the function of the protein with astemizole, which is a known "Merg1a channel blocker." The researchers found that the drug produced basically the same results as the gene therapy. In fact, muscle size increased in mice in the group that were given the drug without any other treatment.
"We are now looking at the differences in the structure of the heart and the skeleton to give us clues on how to specifically target muscles without the cardiac side effects," Pond said.
A lot of people would love to have the effects of exercise last longer. Also, a method to avoid muscle atrophy with age would have very wide appeal.
There is another drug in development which hopes to prevent atrophy, or muscle loss. Which would be a perfect complimet to a myostatin inhibitor.
So imagine coupiling a potential myostatin inhibitor allowing your muscles to grow without the hinderance of myostatin, AND have the atrophy of muscles not work or unused slowed tremendously. A beautiful combination.
(As a note, there currently are no drugs or supliments on the market that can inhibit myostatin. Wyeth pharmacuticals is currently in stage 2 FDA trials of a myostatin inhibitor. It is a pill that disolves in the body...myostatin is a type of protein and the pill is a cellular docking point for the myostatin protein..basically it disolves in the body to "collect" the myostatin..and with less myostatin, muscles have no restrictions on growth from myostatin. Any company claiming to have a myostatin inhibitor is completley fradulent at this time)
Researchers in Purdue University's School of Medicine have discovered genetic and drug-treatment methods to arrest the type of muscle atrophy often caused by muscle disuse, as well as aging and diseases such as cancer.
The findings might eventually benefit people who have been injured or suffer from diseases that cause them to be bedridden and lose muscle mass, or sometimes limbs, due to atrophy, said Amber Pond, a research scientist in the school's Department of Basic Medical Sciences.
"We've found a chemical 'switch' in the body that allows us to turn atrophy on, and, from that, we also have learned how to turn atrophy off."
A protein called Merg1a plays a key role in allowing or blocking muscle atrophy and atrophy can be blocked by an antihistamine which targets Merg1a and also by gene therpy.
The research team found atrophy of skeletal muscle in mice could be inhibited with both gene therapy and drug treatment using astemizole (as-TEM-uh-zole), an antihistamine. This new insight has potential in many different areas of research, Pond said.
"We have discovered a direct link between atrophy and a protein in the skeletal muscle," Pond said. "This led us to develop methods that would block the protein's ability to cause atrophy. Through drug treatment, we were able to block atrophy, allowing muscle to retain 97 percent of its original fiber size in the face of atrophy."
While the drug used in the experiment isn't suitable for human use this discovery points toward a direction for drug development to prevent muscle atrophy with cancer, age, or low exercise.
A mutant form of Merg1a inserted with gene therapy prevented muscle atrophy in low exercise mice.
This method allowed the scientists to demonstrate the effects of skeletal muscle atrophy and investigate reasons for the link with the Merg1a protein. The Merg1a protein is a channel that normally passes a small electrical current across the cell.
The researchers implanted a gene into the skeletal muscle that resulted in a mutant form of this protein that combines with the normal protein and stops the current. The researchers found that the mutant protein would inhibit atrophy in mice whose ability to use their back legs was limited.
Because gene therapy is not yet a practical treatment option in humans, the researchers decided to go a step further and stop the function of the protein with astemizole, which is a known "Merg1a channel blocker." The researchers found that the drug produced basically the same results as the gene therapy. In fact, muscle size increased in mice in the group that were given the drug without any other treatment.
"We are now looking at the differences in the structure of the heart and the skeleton to give us clues on how to specifically target muscles without the cardiac side effects," Pond said.
A lot of people would love to have the effects of exercise last longer. Also, a method to avoid muscle atrophy with age would have very wide appeal.
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